Malignant
glioblastoma is one of the most common malignant
tumors in the neurological system.
Tubeimoside V (1), a new cyclic
bisdesmoside from tubers of Bolbostemma paniculatum, appears to exhibit various
biological activities, including antitumor effect, but the function and mechanism of this new agent on
glioblastoma cells has not previously been determined. In the present study, we investigated the proliferation change of human
glioblastoma U87MG cells exposured to different concentrations (0.9-14.8 microM) of
Tubeimoside V (1) for a certain time. The results showed that
Tubeimoside V (1) significantly suppressed U87MG cell proliferation in a time- and dose-dependent manner (IC(50) = 3.6 microM). Flow cytometric analysis of
DNA in U87MG cells showed that
Tubeimoside V (1) induces the prominent appearance of a sub-G1 peak in the cell cycle suggestive of apoptosis. Furthermore, U87MG cells' treatment with
Tubeimoside V (1) resulted in nuclear condensation with apoptotic bodies observed by both fluorescence and electron microscopy. The result of
annexin V/PI assay showed that
phosphatidylserine externalization began
after treatment, and then increased in the following 24h. Molecular changes explored through Western-blot staining showed
Tubeimoside V (1) decreased the expression levels of Bcl-2
protein and increased the expression levels of
Bax protein. The novel findings suggest that the cytotoxic actions of
Tubeimoside V (1) toward U87MG cells result from the induction of cell apoptosis. Overall, our data demonstrate that
Tubeimoside V (1) is an efficient apoptotic killing agent of
glioblastoma cells and suggest that this mechanism may play a critical role in anti-
tumor chemotherapy.